在主动和被动吸烟中暴露于纸烟烟雾的气相与微粒相成份的重要性

在两个实验的研究中,调查了吸烟者吸入主流烟雾(MS)和不吸烟者吸入了环境烟雾(ETS)中的气相和微粒相成份。通过测定血浆和尿中碳氧血红蛋白(COHb)、尼古丁和古丁素的含量,来确定烟雾吸收的量,可获得的资料是和尿中排泄的硫醚类和诱变活性有相关关系。吸烟者在8小时内吸收了24支烟的全部MS,观察到所有的生化参数都增高.然而,发现在类似的情况下吸入了主流烟雾的气相后,仅有COHb增高,而尿中硫醚类仅轻度增高。不吸烟者暴露于ETS的气相或在同样高的浓度下暴露于整体ETS8小时,引起血浆中的COHb同样增高,而血浆中的尼古丁和古丁素及尿中排泄的尼古丁和硫醚类都比吸烟者低得多。在两种ETS暴露情况下,尿中诱变性并未发现升高.本文作者的结果表明,最常用于吸烟烟雾吸收的生物指标(尼古丁和古丁素一方面指出吸烟者是暴露于微粒成份,而另一方面被动吸烟者是暴露于气相成分。被动吸烟的微粒暴露似乎是低的,而显示ETS微粒暴露的生物指标迄今尚未找到。这些发现强调指出从主动吸烟推断到被动吸烟的危险性,仅根据纸烟当量或某一生物指标(如:古丁素)来判断可能导致错误。     

被动吸烟者尿中尼古丁含量的测定

本次调查在冬季选用了一长途火车上的１０名列车员，收集了他们２４小时的尿液，对尿中尼古丁及其衍生物的含量进行测定。结果发现这１０名被动吸烟者尿中尼古丁及其衍生物的含量明显高于完全无被动吸烟者且差异有非常显著性。可见被动吸烟对人体健康的影响是不容忽视的。     

被动吸烟暴露评价的常用方法

被动吸烟的危害越来越被关注,掌握被动吸烟暴露评价方法对保证相关研究科学开展十分重要。本文对目前被动吸烟暴露评价的常用方法进行了比较,重点介绍了目前用于检测被动吸烟的4种常用方法:问卷调查法、室内空气中尼古丁测定法、室内空气细颗粒物测定法、人体烟碱代谢产物可替丁测定法,并比较各种方法的优缺点,指导在科研工作中如何进行暴露评价方法的选择。     

被动吸烟对儿童谷胱甘肽过氧化酶活力及VitC的影响

目的：研究被动吸烟对儿童体内谷胱甘肽过氧化物酶活力（ＧＳＨ－ＰＸ）及维生素Ｃ（ＶｉｔＣ）的影响。方法：以整群抽样的方法调查了９６４名儿童，从中筛选出家中无吸烟者、家中一人吸烟及两人以上吸烟儿童各２０名。为避免主观误差，我们以尼古丁代谢产物可铁宁作为吸入烟雾多少的客观指标，同时测定血清中谷胱甘肽过氧化物酶活力及尿中维生素Ｃ含量。结果：可铁宁与被动吸烟量直接相关。而ＧＳＨ－ＰＸ及ＶｉｔＣ随着吸入烟雾浓     

云南省云县不同性别人群吸烟及被动吸烟调查

目的过问卷调查了解云南省云县不同性别吸烟和被动吸烟状况。方法采用分层随机抽样方法进行问卷调查。对不同性别人群吸烟状况、吸烟开始年龄、平均每日吸烟量、被动吸烟率、被动吸烟开始年龄、被动吸烟暴露量等指标进行分析。结果被调查的1002人中,总吸烟率为34.83%,男性吸烟率为71.46%,女性吸烟率为2.08%。开始吸烟的平均年龄为(19.00±5.23)岁,日平均吸烟量为(17.60±11.13)支。被调查者中非吸烟者的被动吸烟率为86.37%,男性被动吸烟率为79.25%,女性为88.22%。在被动吸烟的564人中,从出生就暴露于环境烟雾的有291人,占被动吸烟者的51.60%;被动吸烟者平均每天暴露时间为(3.98±3.43)h,女性被动吸烟者中平均每天暴露时间为(4.11±3.60)h。结论男性吸烟率与吸烟量偏高,开始吸烟年龄小;女性是被动吸烟的主要人群,女性的被动吸烟率高,日平均暴露量大,暴露年限长。     

被动吸烟者吸入暴露的研究

按国际标准组装的模拟吸烟装置和测试方法,对4种纸烟主流烟气和侧流烟气中的焦油、尼古丁、~(210)Pb和~(210)Po含量进行测试,并估算了被动吸烟者的吸入暴露,与吸烟者比较。中等吸烟环境二者比值约为1/7～1/8。人员密集和吸烟人数多时,比值可达1/1.2。认为在号召戒烟的同时,应限制在公共场所吸烟。     

乳腺癌与主动和被动吸烟的关系

关于被动吸烟的研究一致表明被动吸烟增加乳腺癌的危险，而关于主动吸烟的研究没有表明这种联系。这一明显的矛盾是由于在评价主动吸烟的影响时，没有将被动吸烟者与本暴露者分开。为了确定主动吸烟与被动吸烟对乳腺癌的影响，1992年1月～1993年10月在瑞士日内瓦进行了人群的病例对照研究，其中未暴露包括未主动和被动暴露于吸烟的女性。244例乳腺癌患者，与IO32例非乳腺癌女性进行对比。逐年记录Ic岁至调查日期之间的主动与被动吸烟史。曾主动吸烟的乳腺癌患者与从未主动与被动吸烟的女性相比，日均吸烟l～9支者调整的OR一2．2（95％可信…     

主动和被动吸烟对妇女妊娠过程及其子女红细胞系统生成的影响

本文研究了主动和被动吸烟对妇女妊娠过程和泌乳机能的影响,以及幼儿接触尼古丁烟气其红细胞代谢、铁代谢、血红蛋白成分的特点。受检者为年龄1岁的幼儿119名,第1组22名,其父母或母亲是吸烟者。第2组74名,其父亲是吸烟者。对照组23名,其家庭无吸烟     

云南罗平县农村居民烟草暴露及尼古丁依赖调查

目的 了解云南省罗平县农村居民烟草暴露与尼古丁依赖现状。方法 采用按比例概率抽样方法抽取当地12个乡镇≥18岁居民4 611人进行调查。结果 罗平县农村居民吸烟和被动吸烟率分别为40.0%(1 844/4 611)和27.8%(1 281/4 611),其中男性吸烟率为79.2%,女性为1.2%,男性被动吸烟率为8.8%,女性为46.6%,男性吸烟率明显高于女性(P<0.01),而女性被动吸烟率明显高于男性(P<0.01);村民中度及以上尼古丁依赖率为51.1%,家庭种烟者和高收入者(年收入≥15 000元)的吸烟率分别为44.5%和44.1%,明显高于家庭不种烟者和低收入者的37.4%和35.4%,(P<0.01);文化程度初中及以下被动吸烟率为42.9%,高中及以上为24.1%,被动吸烟率随着文化程度的增加而减少(P<0.05);农村居民以吸过滤嘴香烟为主(63.6%),其次为水烟袋(53.4%);初次吸烟年龄主要集中在15~24岁组的青年人群(93.0%),吸烟者中在过去12个月内尝试戒烟1次的比例仅为13.4%,过去7 d内被动吸烟场所在主要集中在家里和公共场所的比例分别为97.0%和88.5%。结论 罗平县村民吸烟和被动吸烟情况较严重,应重点加强家庭种烟者、男性和低文化程度人群的控烟工作。     

咸宁城区被动吸烟人群尿中可替宁和3-羟基可替宁的检测

目的探讨咸宁城区被动吸烟人群被动吸烟量与尿中可替宁、3-羟基可替宁浓度的关系,准确评价被动吸烟人群烟草暴露水平,为政府制定控烟政策提供科学依据。方法根据被动吸烟指数等级分为3组,1～9、10～19和≥20支/天,采集咸宁城区被动吸烟人群尿样共120份(每组40份),另外,采集咸宁市疾病预防控制中心工作人员中本人不吸烟,且最近3个月无烟草暴露史的40人作为空白对照,对其工作生活环境等情况进行问卷调查。利用气相色谱-质谱检测法测定尿中2种尼古丁的代谢产物可替宁、3-羟基可替宁的含量,并对结果进行统计分析。结果被动吸烟量与尿液中的可替宁和3-羟基可替宁浓度均呈正相关(r=0.872、0.745,均P<0.01)。随着被动吸烟量的增加,尿液中可替宁、3-羟基可替宁含量均升高。结论被动吸烟可以增加尿液中可替宁、3-羟基可替宁的含量,可替宁和3-羟基可替宁可以作为反映被动吸烟人群烟草暴露水平较好的标志物。     

Studies on a simultaneous analytical method of urinary nicotine and its metabolites, and their half-lives in urine

The objectives of this research were to improve and standardize a relatively easy, highly sensitive and highly accurate method of measuring nicotine, cotinine and trans-3'-hydroxycotinine in the urine of non-smokers exposed to environmental tobacco smoke (ETS) and to clarify the reliability of this method. Blinded studies using this analytical method were conducted in two universities. Standard solutions of nicotine, cotinine and trans-3'-hydroxycotinine were prepared at one university, divided in two parts and sent to another two universities for analyses by gas chromatography-mass spectrometry (GC/MS) without revealing the concentrations. It was found that the assay lower limit was at a level that could be used in passive smoking surveys and good results were obtained in crosschecks of samples of unknown concentration between the two universities. Since this method was considered to be useful for analyzing these urinary substances, ETS exposure experiments were performed in three universities using urinary nicotine, cotinine and trans-3'-hydroxycotinine as specific biomarkers of the urine. Non-smokers were exposed to ETS in an exposure room in each university. It was found that the nicotine concentrations in the urine of the subjects exposed to ETS reached a peak at about 2 hours after the end of exposure, which was somewhat later than that in active smokers. Because cotinine and trans-3'-hydroxycotinine in the urine are metabolites of nicotine, it was evident that the quantities were lower and the increasing rates were also less than that of nicotine. When the deceases in nicotine/ creatinine, cotinine/creatinine and trans-3'-hydroxycotinine/creatinine ratios in the urine were calculated using theoretical curves, the half-life times were calculated to be 13.9, 20.0 and 63.0 hours, respectively.     

Active and passive exposure status to tobacco smoke of department store employees measured by cotinine ELISA

Quantitation of urinary cotinine, a major metabolite of nicotine, by an enzyme-linked immunosorbent assay (ELISA), was performed in parallel with questionnaires containing items on smoking status, such as active and/or passive smokers, the number of cigarettes smoked, and the presence or absence of active smokers in the surroundings in a department store (517 employees). The cotinine values corrected by creatinine (cotinine-creatinine ratios, CCRs) approximately conformed to the extent of self-recognition of their exposure status to tobacco-smoke, and were low in the order of active smokers, passive smokers and non-smokers who felt they were not exposed to tobacco-smoke. Occupational differences of the CCRs were not found in the employees. In the active smokers, the CCRs were increasing according to the number of cigarettes per day they smoked, and the values were nearly proportional to nicotine contents of cigarette in the moderate smokers who smoked 11-20 cigarettes per day. The CCRs of males were higher than those of females in the active smokers, which also agreed well with the numbers of cigarettes they smoked per day. In the passive smokers, the CCRs were remarkably and significantly higher in subjects who felt they were exposed to tobacco-smoke both in their workplaces and homes. Urinary CCRs measured by ELISA are thus found to be a reliable and excellent objective indicator of both active and passive exposure-status to tobacco-smoke.     

Respiratory effects of lowering tar and nicotine levels of cigarettes smoked by young male middle tar smokers. II. Results of a randomised controlled trial.

STUDY OBJECTIVE--The aim was to investigate the effect on respiratory health of male middle tar smokers changing the tar and nicotine levels of the cigarettes they smoke for a six month period. DESIGN--This was a randomised controlled trial. Middle tar smokers were randomly allocated to smoke one of three different types of cigarette (low tar, middle nicotine; middle tar, middle nicotine; and low tar, low nicotine) in place of their usual cigarette for a six month period. Main outcome measures were assessment of respiratory health by documenting respiratory symptoms and peak expiratory flow rates, and of nicotine inhalation by measuring the urinary excretion of nicotine metabolites. SETTING--21 local authority districts of England. SUBJECTS--Participants were male middle tar smokers aged 18-44 years. MAIN RESULTS--Changes in the measures of respiratory health showed little difference over the trial period between the three cigarette groups. Analyses of the urinary nicotine metabolites showed that smokers allocated to each of the three study cigarettes adjusted their smoking so that throughout the trial their nicotine inhalation differed little from their pretrial intakes when they were smoking their own cigarettes. As a result of the altered patterns of smoking to compensate for the reduced nicotine yields of the three study cigarettes, the tar intake of those allocated to smoke the middle tar, middle nicotine cigarettes remained essentially unchanged, while those allocated to smoke the low tar, low nicotine and low tar, middle nicotine cigarettes had calculated reductions in tar intakes of about 14% and 18%, respectively. CONCLUSIONS--Due to the phenomenon of compensation, tar intake can only be reduced substantially by using a cigarette with a markedly lower tar/nicotine ratio. Nevertheless reductions of up to about 18% in tar intake failed to result in any detectable effect on respiratory symptoms or peak expiratory flow rates over a six month period.     

Tobacco sidestream smoke: Uptake by nonsmokers

Some epidemiological studies indicate an association between passive smoking and an increased risk for cancer, especially for cancer of the lung. Other reports, however, have failed to confirm these findings. Biochemical analyses of the physiological fluids for markers of exposure to tobacco smoke are needed as measurements of the uptake of smoke components by nonsmokers and for the estimation of relative cancer risk to passively exposed persons compared with that to active cigarette smokers. This communication reports the uptake of carbon monoxide, hydrogen cyanide, and nicotine after passive smoke exposure under controlled conditions. The results indicate that salivary nicotine values reflect the level of recent passive smoke exposure within an hour and that urinary cotinine values indicate the level of passive smoke exposure in the preceding hours. N-Nitrosoproline has been shown to serve as an indicator of endogenous N-nitrosamine formation in cigarette smokers: yet, preliminary studies do not indicate that urinary excretion of N-nitrosoproline is increased following short-term passive smoke exposure. In infants, first field studies suggest a correlation between exposure to tobacco-smoke-polluted environments and levels of cotinine in both serum and urine.     

吸烟的生化标记—尿尼古丁代谢产物的测定

A novel, barbituric acid method of detecting urinary nicotine metabolites was evaluated for use as an objective test of smoking. Urine samples were collected from 289 male smokers and 167 male nonsmokers. The smokers recorded the number of cigarettes smoked on the previous day. This method correctly classified the subjects as smokers or nonsmokers. There was a significant positive correlation (r = 0.587, P less than 0.001) between the urinary nicotine metabolites/creatinine ratios and number of cigarettes smoked. This method can be performed very rapidly and reagent costs are very cheap. It is a good objective test of smoking and nicotine intake.     

Passive smoking under controlled conditions

Summary Ten healthy subjects were exposed to passive smoking at a high level corresponding to 25–30 ppm CO in the ambient air for 3 h. All subjects were exposed at the same time in a climatic chamber especially designed for exposure experiments. Despite an identical exposure rate considerable interindividual variability of subsequent nicotine and cotinine levels in saliva, plasma and 24-h urine were observed. This variability was more prominent in nicotine than in cotinine levels. The kinetic pattern as reflected by saliva levels for up to 24 h was consistent with previous data found in active smokers. Nicotine levels found in saliva were markedly influenced by repeated sampling. This was not the case for cotinine levels. With regard to laboratory techniques RIA seems to be more sensitive than gaschromatography (GC). The results of this study suggest that measuring cotinine levels in 24-h urine with RIA is presently the most sensitive and reliable criterion for estimating exposure to passive smoking and for validating questionnaires or interviews about short-term exposure to passive smoking.     

The influence of passive smoking on the cardiovascular system

Cardiovascular effects of tobacco smoke have been studied in passive smokers far less extensively than in active smokers. Under real-life conditions, passive smokers inhale approximately 0.02 to 0.01 of the amount of particulate matter taken up by active smokers. Their nicotine concentration in serum is within a range that is barely distinguishable from the background level. The increase in carboxyhemoglobin rarely exceeds 1%. In healthy subjects heavily exposed to tobacco smoke, no or only slightly acute effects on the cardiovascular system are found. Whether or not passive smoking is likely to aggravate symptoms in patients with advanced coronary heart disease has not yet been unequivocally established and requires further investigation. From a few studies on occupational groups exposed to carbon monoxide (CO) and from experiments with animals chronically treated with CO or nicotine, the conclusion can be drawn that neither CO nor nicotine is likely to play a role in the development and progression of coronary heart disease in those concentrations normally found in passive smokers.     

Importance of exposure to gaseous and particulate phase components of tobacco smoke in active and passive smokers

Summary The uptake of tobacco smoke constituents from gaseous and particulate phases of mainstream smoke (MS), inhaled by smokers, and of environmental tobacco smoke (ETS), breathed in by non-smokers, was investigated in two experimental studies. Tobacco smoke uptake was quantified by measuring carboxyhemoglobin (COHb), nicotine and cotinine in plasma and urine and the data obtained were correlated with urinary excretion of thioethers and of mutagenic activity. An increase in all biochemical parameters was observed in smokers inhaling the complete MS of 24 cigarettes during 8 h, whereas only an increase in COHb and, to a minor degree, in urinary thioethers was found after smoking the gas phase of MS under similar conditions. Exposure of non-smokers to the gaseous phase of ETS or to whole ETS at similar high concentrations for 8 h led to identical increases in COM, plasma nicotine and cotinine as well as urinary excretion of nicotine and thioethers which were much lower than in smokers. Urinary mutagenicity was not found to be elevated under either ETS exposure condition. As shown by our results, the biomarkers most frequently used for uptake of tobacco smoke (nicotine and cotinine) indicate on the one hand the exposure to particulate phase constituents in smoking but on the other hand the exposure to gaseous phase constituents in passive smoking. Particle exposure during passive smoking seems to be low and a biomarker which indicates ETS particle exposure is as yet not available. These findings emphasize that risk extrapolations from active smoking to passive smoking which are based on cigarette equivalents or the use of one biomarker (e.g. cotinine) might be misleading.     

Relationship between environmental tobacco smoke and urinary cotinine levels in passive smokers at their residence

Studies of the health effects of environmental tobacco smoke (ETS) using measured air concentrations are subject to bias. Cotinine, a nicotine metabolite detected in urine, has been recommended as a quantitative measure of nicotine intake and thus as a marker for ETS exposure in humans. The aim of this study was to correlate home indoor ETS levels with passive smokers' urinary cotinine levels. The urinary cotinine concentrations of 57 non-smoking women who spend >19 h a day at home and the nicotine levels in their living room air were measured over a period of 24 h. Nicotine and urinary cotinine levels were analyzed using GC/MS and HPLC/UV, respectively. In addition, information was collected regarding the smoking habits of the subjects' families. A significant correlation was found between the nicotine levels in indoor air and the urinary cotinine to creatinine ratio of the passive smokers. The smoking habits of the subjects' family members were also correlated to the urinary cotinine levels of the passive smokers.     

The urinary mutagenicity test in monitoring exposure to aromatic polycyclic hydrocarbons in workers in the aluminum industry]

The sensitivity of 3 urinary mutagenicity tests was assayed: the plate test, the fluctuation test and the micropreincubation test, in order to assess their possible use in monitoring human exposure to polycyclic aromatic hydrocarbons (PAH). Urine samples from workers of an anode production plant exposed to coal tar and from psoriatic patients undergoing treatment with coal-tar ointments were tested for mutagenic activity on strain TA98 Salmonella typhimurium, in the presence of the microsome fraction and deconjugating enzymes. Parallelly, the urinary concentration of PAH metabolites or one of their trace metabolites, 1-hydroxypyrene, was determined. Increased levels of PAH metabolites were observed in the urine of anode production workers after a work shift compared with controls. Results of the plate test and the fluctuation test performed on urine of exposed subjects, both smokers and nonsmokers, showed mutagenicity values similar to the controls. Much higher 1-hydroxypyrene concentrations were found in the urine of psoriatic patients treated with coal tar than in post-shift urine of anode production workers. The urine of the former was also mutagenic in the 3 mutagenicity tests used. The minimum mean dose of PAH metabolites was calculated, expressed as quantity of 1-hydroxypyrene, that would give a mutagenic response in the 3 tests: the micropreincubation test was found to be about 100 times more sensitive than the plate test and about 30 times more sensitive than the fluctuation test. The theoretical minimum urinary concentration of 1-hydroxypyrene detectable by each test was determined: the micropreincubation test was 15 times more sensitive than the plate test and 7 times more sensitive than the fluctuation test.(ABSTRACT TRUNCATED AT 250 WORDS)